Hypothesis: leukocyte endogenous mediator/endogenous pyrogen/lymphocyte-activating factor modulates the development of nonspecific and specific immunity and affects nutritional status.
We postulate that leukocyte endogenous mediator/endogenous pyrogen/lymphocyte-activating factor (LEM/EP/LAF) integrates the host's nonspecific and specific immune responses to infection by virtue of the panoply of physiological and metabolic activities it is capable of eliciting. The alterations in systemic metabolism modulated by LEM/EP/LAF, although apparently of value to the host in the defense against infection and the repair of tissue damage, result in negative nutrient balances. Severe infections, alone or in conjunction with injury, may result in malnutrition unless the patient is adequately nourished. Preexisting nutritional deficits can compromise host resistance to infection, in part by preventing production of LEM/EP/LAF. Additional studies of the sequelae of LEM/EP/LAF action and effects of nutrition on host resistance to infection appear warranted.
D006801:Humans; D007111:Immunity, Cellular; D007113:Immunity, Innate; D007239:Infections / Q000150:complications / Q000209:etiology / Q000276:immunology* / Q000378:metabolism; D007375:Interleukin-1; D008099:Liver / Q000276:immunology; D009748:Nutrition Disorders / Q000150:complications / Q000209:etiology / Q000276:immunology*; D010586:Phagocytes / Q000276:immunology; D011506:Proteins / Q000276:immunology*; D011749:Pyrogens / Q000276:immunology*
D007375:Interleukin-1; D011506:Proteins; D011749:Pyrogens; C008270:leukocyte endogenous mediator